Management of Brain Injury After Resuscitation From Cardiac Arrest

Abstract

About 460,000 sudden cardiac deaths from a total of 728,743 cardiacrelated deaths were reported in 1999 in the United States [1]. Thirty-six percent of the sudden deaths were in-hospital cardiac arrest and 64% were out-of-hospital arrest [1]. About 18% of patients survive to discharge following in-hospital cardiac arrest [2,3], whereas only 2% to 9% of patients who experience out-of-hospital cardiac arrest survive to discharge [4][5][6]. Functional outcomes of survivors are variable, but poor-quality survival is common [7], with only 3% to 7% able to return to their previous level of functioning [8]. The prevalence of coma or persistent vegetative state among survivors represents an enormous burden on patients, their families, health care personnel, and resources. The economic impact of cardiac arrest was the subject of a cost-effectiveness study that compared continuing versus withholding cardiopulmonary resuscitation (CPR) and ventilatory support after day 3. The estimated incremental cost of the more aggressive care strategy was $140,000 (1998 dollars) per quality adjusted life year (QALY) for high-risk patients (three to five risk factors, 93% 2-month mortality) and

Fatty acid methyl esters as a potential therapy against cerebral ischemia

“…Cardiac arrest (a form of global cerebral ischemia) occurs when CBF to the brain and other organs is stopped or drastically reduced (Geocadin et al, 2008;Huang et al, 2014;Stub et al, 2011). If circulation is restored in a short period of time neurological symptoms may be transient.…”

“…However, at times, brain damage may be permanent and irreversible if a significant amount of time passes (more than 5 min) before restoration of CBF. The most common causes of cardiac arrest in 60-70% of cases are ventricular fibrillation or ventricular tachycardia due to ischemic heart disease (Geocadin et al, 2008;Huang et al, 2014;Stub et al, 2011). The most critical factors determining overall patient survival during cardiac arrest are effective CPR, prompt cardiac rhythm analysis, and early defibrillation in cases of ventricular fibrillation.…”

“…The most vulnerable areas to hypoxic injury are the CA1 region of the hippocampus; layers 3, 5 and 6 of the cerebral cortex, and cerebellar Purkinje cells (Geocadin et al, 2008). Global cerebral ischemia results in widespread neuronal damage via loss of adenosine triphosphate (ATP) production leading to dysfunction of Na + /K + ATPase pumps.…”

“…Reperfusion provides oxygen as a substrate for several enzymatic oxidation reactions that produce free radicals, increasing excitotoxicity. These reactive oxygen species are known to cause damage through lipid peroxidation, protein oxidation, and DNA fragmentation, all contributing to neuronal apoptosis (Geocadin et al, 2008;Stub et al, 2011).…”

“…injecting cold fluids and the use of ice pack surrounding the patient to lower body temperature to 32-34 • C (Geocadin et al, 2008)), the use of intravenous thrombolytic agents, such as recombinant tissue plasminogen activator, is standard therapy for ischemic stroke within 3 h after the onset of symptoms (The National Institute of Neurological Disorders, 1995;Wardlaw et al, 2014). Thrombolytics dissolve the arterial brain clot reestablishing CBF, protecting neurons from damage while improving neurological function (1995; Wardlaw et al, 2014).…”